Download continuum versus dichotomy in theories of schizophrenia`

262
SCHIZOPHRENIA BULLETIN
continuum versus dichotomy in theories of schizophrenia'
Philippe Khouri
"The etiology common to the onset of a psychoneurosis and of a psychosis always remains the same...."
Sigmund Freud, "Neurosis and Psychosis"
(1924), Standard Edition, 1953, p. 152.
There is a sharp difference of opinion in the psychiatric literature over whether schizophrenic disorders exist on a continuum with other mental disorders
and normality, but this issue has in the past been overshadowed by another controversy—the role of genetic
vs. environmental factors in the etiology of schizophrenia. This paper argues that the division of theories
of schizophrenia into those emphasizing genetic and
those emphasizing environmental factors overlooks
similarities between certain genetic and certain environmental models. Arranging the theories of schizophrenia according to the concept of a continuum of
disorder allows for a new perspective, by which monogenic theorists (e.g., Book 1953, Heston 1970, Kallmann 1946, and Slater and Cowie 1971) and certain
environmental theorists (e.g., Alanen 1966 and Lidz
1973) form one group; while proponents of polygenic
models (Gottesman and Shields 1973) and other environmental theorists (e.g., Bateson et al. 1956 and
M. Bleuler 1965 and 1972) form a second group.
The concept of a continuum of schizophrenic disorders is interpreted in various ways. A t times, it is
used in the context of phenomenology. This type of
continuum refers to the lack of symptom specificity
in schizophrenia—a lack that has been cited by
Kraepelin (1971), Meyer (1948), Sullivan (1974), M.
Bleuler (1965), and more recently Strauss and Carpenter
* Reprint requests should be addressed to the author at
Rm. 2N-220A, Bldg. 10, NIMH, 9000 Rockville Pike, Bethesda,
Md. 20014.
(1974). A contrasting position has been taken by Schneider (1959) who views certain symptoms as specific and
pathognomonic to schizophrenia. At other times, the
concept of a continuum is applied to the outcome or
prognosis of schizophrenic disorders. This type of continuum refers to a variability in outcome possibilities in
contrast to a unidirectional deteriorative outcome for
schizophrenia (E. Bleuler 1950, M. Bleuler 1972, Meyer
1948, Strauss and Carpenter 1974, and Sullivan 1974).
Etiological Continuum vs.
Etiological Dichotomy
Another context for the use of a continuum of
schizophrenia disorders is etiology. In the following discussion the concepts of an etiological continuum and
its opposite, an etiologicai dichotomy, will be explored.
Those who hypothesize an etiological dichotomy posit
the presence of specifiable etiological factors which
operate in schizophrenia but not in other disorders.
Some other theorists assume that there are no such
specific factors. They postulate a number of relevant
etiological factors with which the nonschizophrenic
population has often had contact. Thus, they hypothesize an etiological continuum; Though for genetic
theorists these factors are the "schjzophrenogenic"
genes and for the environmental theorists these factors
are a variety of influences (often interpersonal), the common underlying assumption of the etiological continuum
models is that any difference that exists between schizophrenics and nonschizophrenics is more quantitative
than qualitative. In other words, people become
schizophrenic because they. have too many of the
schizophrenogenic factors; there are members of the
population who have had some—but not enough—of
these factors and thus escaped having the illness. The
263
VOL.3, NO. 2,1977
polygenic/multifactorial model of inheritance, as proposed by Gottesman and Shields (1973), is an example
of a genetic continuum model, while the double-bind
theory of Bateson et al. (1956) and the theory of M.
Bleuler (1965 and 1972) are examples of environmental
continuum models.
Theories of an etiological dichotomy posit a qualitative breach between schizophrenics ai.d nonschizophrenics because putative factors in the etiology of
schizophrenic disorders, whether genetic or experiential, are said not to occur in the nonschizophrenic
population. The monogenic/major gene hypothesis of
disease transmission proposed by Slater and Cowie
(1971), Heston (1970), and others exemplifies a dichotomous genetic model. Lidz's (1973) "Schizophrenic
families" theory and Alanen's (1966) similar hypotheses
are examples of dichotomous environmental models.
The sampling of theorists who emphasize environmental factors is small because for many theorists it
was difficult to find answers to the specific question
asked: Are the etiological factors important in schizophrenia found also among nonschizophrenics, or are
they limited to schizophrenics? One possible explanation
for this difficulty is that some environmental theorists
tend to focus on the individual and his immediate human environment. They attempt to answer the question: What made this person ill? They do not often concern themselves with what has become of others who
may have had these same adverse influences (Arieti
1975). However, it was possible to find answers to this
question (or at least allusions to it) in the writings of
Bateson et al. (1956), M. Bleuler (1965 and 1972), Lidz
(1973), and Alanen (1966)—some of the most prominent contemporary writers on schizophrenia.
In table 1, genetic and environmental theorists are
grouped according to their shared assumptions regarding
an etiological continuum. These assumptions are either
stated clearly or implied in their writings. Within a
group, investigators may have (and frequently do have)
drastically different views on the phenomenology, outcome, or "nature" of schizophrenia; but an attempt is
made to present evidence that, despite these differences,
they share common assumptions about the specificity
or lack of specificity of etiological factors.
Etiologically Dichotomous Models
Proponents of this type of etiological model have
Table 1. Genetic and environmental etiological
models of schizophrenia from the continuum/
dichotomy perspective
Model
Genetic
Specificity/
dichotomous
Nonspecificity/
continuum
Monogenic/major
gene hypothesis,
e.g.. Book (1953),
Heston (1970).
Kallmann (1946),
Slater and Cowie
(1971)
Polygen ic/mu Itif actorial
hypothesis, e.g., Gottesman and Shields (1973),
Reich et al. (1972 and
1975)
Environ- Schismatic and
mental
skewed families,
e.g., Lidz (1973)
Chaotic and restricted families,
e-g., Alanen (1966)
Disharmony of personality tendencies,
e.g., M. Bleuler (1972) 1
Double-bind situation,
e.g., Bateson etal.(1956)
1
M . Bleuler's interactional model assumes that both genetic
and environmental factors are nonspecific, the genetic predisposition being a disharmony of "normal" genes rather than
pathological genes.
tended to conceptualize in terms of "schizophrenia"
or "schizophrenic" rather than the "schizophrenias"
or "schizophrenic disorders." Though variation in the
clinical picture is recognized, a unifying factor is presumed to exist—that of etiology. Kraepelin began this
tradition by stating that hebephrenia, catatonia, and
paranoia should be grouped together and put aside from
other disorders because they were all products of the
same etiology. Kallmann (1946), Book (1953), Heston
(1970), and Slater and Cowie (1971) have similar
views, presenting a genetic abnormality as the etiological
factor. The major gene hypothesis as proposed by these
theorists may be described as follows:
• Schizophrenia is a disease that has a genetic basis.
The genetic basis is an autosomal gene with variable
penetrance. (There is disagreement as to whether this
autosomal gene is dominant or recessive.)
• Not all individuals who have the schizophrenogenic gene become schizophrenic. In Slater and Cowie's
(1971) model all homozygotes and 22 percent of heterozygotes are expected to manifest schizophrenia. The
264
phenotypic fate of those heterozygotes who do not develop schizophrenia is thus a problem. One answer has
been to attempt to find cases of "near-schizophrenia"
variously described as "eccentric personalities," "schizoid psychopaths" (Kallmann 1946), or "schizoid personalities" (Heston 1970).
• The presence of this major gene is necessary for
the development of schizophrenia. Individuals who do
not have the schizophrenogenic gene do not become
schizophrenic regardless of the presence of modifying
genes or environmental stresses. Thus, there is a qualitative difference between schizophrenics and the rest
of the population by virtue of the presence of schizophrenogenic genes.
Lidz (1973) and Alanen (1966), who argue from the
environmentalist side, appear to reach a similar conclusion about etiological specificity, though they might
object to being grouped with some of those listed above.
In his latest book on schizophrenia, Lidz (1973) articulates his approach clearly. He starts by stating that
"a great deal concerning the etiology of schizophrenic
disorders is now firmly established" (p. 6). He then
proceeds to refute any specific genetic basis for schizophrenia and develops his theory, based on observations (not controlled clinical studies) of families of
schizophrenics whom he has followed over several
years. His conclusions could be summarized as follows:
• Schizophrenia is "one of the potential fates to
which man is subject... due to . . . the many potential
hazards that beset his path from infancy to maturity"
(P-6).
• One of those hazards is exposure to a schizophrenogenic family. The family is the medium for the
acquisition of language and socialization skills. Disturbances in these areas characterize the disorders
called "schizophrenia."
• Not all kinds of "flawed and deprived" family
settings are responsible for schizophrenia-only "specific distorting influences" make a family schizophrenogenic (p. 23). He describes these "influences" in
terms of schismatic and skewed families and gives
clinical examples.
• In this model, schizophrenics differ from nonschizophrenics in a qualitative sense because of the
specific nature of the etiological factors to which they
have been exposed. Schizophrenic offspring are found
only in schismatic and skewed families (p. 49).
• The specificity of etiological factors is such that
SCHIZOPHRENIA BULLETIN
only schizophrenia develops in the offspring rather than
other psychopathological conditions (p. 23).
Alanen (1966) investigated the families of 30 schizophrenics and those of 30 neurotics. He found a qualitative difference between the family disturbances in the
two series—10 "chaotic" families in the schizophrenia
series as compared to none in the neurosis series. From
this dissimilarity, he came to his conclusions about
etiological factors. His position may be summarized as
follows:
• There is no need to invoke any specific genetic
predisposition (i.e., monogenic transmission). If any
genetic basis exists, it is "diffuse rather than strictly
specific" and may consist "in a heightened inborn
passivity or in an inborn inclination to introversion"
(p. 551).
• "The pathogenetic influences of the family environment" are the critical factors that produced "the
disorders in the children" (p. 547).
• Those pathogenetic influences in the families of
schizophrenics (the etiological milieu) are described as
"chaotic" family interactions reflecting one parent's
intense irrationality and incoherence. These influences
are absent in families with neurotic offspring.
• In reference to etiological specificity, he states:
Thus, evidence is accumulating in support of the
following view: the disorders met in the patients'
environments of growth . . . differ depending on the
disorder type; and they seem to differ to an extent
justifying the conjecture that they are at least comparatively specific, [p. 550]
In conclusion, regardless of whether or not there is
an overlap at the phenomenological level between
schizophrenics and the rest of the psychiatric and nonpsychiatric population, the dichotomous models discussed above do set apart schizophrenics from the rest
of the population at an etiological level, because persons
destined to become schizophrenic are assumed to have
special etiological influences.
Continuum Etiological Models
These etiological models differ from the previous
ones because they do not assume any one factor specific
for the etiology of schizophrenia. The same factors operate in schizophrenics and nonschizophrenics, and
these models emphasize quantitative differences rather
VOL.3, NO.2,1977
265
than qualitative ones.
The polygenic/multifactorial model represents a
genetic continuum model. It is used by Gottesman and
Shields (1973) and Reich and his associates (Reich,
Cloninger, and Guze 1975 and Reich, James, and Morris
1972) to explain the familial distribution of schizophrenia. It uses the normal curve, which plots the distribution of traits like height, weight, and blood pressure—traits that are continuously distributed in the
general population. The concept of the normal curve
has been adapted by these theorists for use with noncontinuous traits such as liability (figure 1). Falconer
(1965) first developed the concept of liability to account for the sum total of genetic and environmental
causes of a disorder—in that case, schizophrenia. The
assumptions of the polygenic model can be summarized
as follows:
• The liability to develop schizophrenia is normally
distributed.
• Schizophrenia appears when its threshold on the
liability scale is passed.
• The heritability of the liability is 85 percent. In
other words, genetic factors are the most important contributing factors for the development of schizophrenia.
• The genetic basis is necessary for the expression of
the disorder and consists of many abnormal genes whose
distribution in the general population is continuous and
normal (statistical sense).
• A corollary of the above assumption is that the
putative abnormal genes exist in persons who are not
schizophrenic, but in a lesser amount. This accounts for
their asymptomatic status.
• From a genetic standpoint, any difference between
Figure 1. The polygenic/multifactorial model1
Mean liability
in the general
population
Frequency
Liability to develop
schizophrenia/threshold
Schizophrenic
phenotypes
^The model shows the distribution of the liability in the general population with one threshold for schizophrenia.
266
schizophrenics and the rest of the population is essentially quantitative rather than qualitative.
Arguing from the environmentalist side, Bateson,
et al. (1956) have presented the double-bind theory as
an alternative etiological model for genetic theories. The
theory represents an environmental continuum model
and assumes the following:
• Schizophrenic symptoms are not a reflection of
disease processes in the medical sense of the word but a
reflection of communicational disturbances between the
" v i c t i m " (in this case the schizophrenic patient) and another member of his family (usually the patient's
mother).
• Schizophrenic disorders appear as a result of a
sequence of experiences that bring about a double-bind
situation in which, whatever the victim does, he is the
loser. The double-bind theory is based on the "theory
of logical types" (Whitehead and Russell 1910), which
stipulates that there is a logical discontinuity between a
class and its members. In the psychology of everyday
communications, an attempt is always made to breach
various levels of communicational modes—for example,
modes of play, fantasy, nonplay, and humor. The schizophrenic-to-be is continuously thwarted by his mother in
his attempts to breach his different communicational
modes in a "normal" and "consensually validated" way.
The mother's attitude reflects her own psychological
difficulties which are of unconscious origin. The symptoms of schizophrenia appear when certain formal
types of breaching are used by the "victim."
• The future schizophrenic is victimized by the
double-bind situation and becomes conditioned to
react to all situations in life as if he were in a double
bind even though he may no longer be exposed to a
double-bind situation. The notion of "a priming time"—
an initial time when the double-bind situation is most
effective—is used to explain the occurrence of this conditioned response when the conditioning stimulus
(double-bind situation) is removed.
• The double-bind situation is a characteristic of
families of schizophrenics, of the relationship between
the preschizophrenic and his mother, and of normal
relationships. Thus (according to Bateson et al.), any
person exposed to a double-bind situation will "respond
defensively in a manner similar to the schizophrenic"
(p. 254).
In conclusion, a rather complex family dynamics—the
double-bind situation—is considered to be causally re-
SCHIZOPHRENIA BULLETIN
lated to schizophrenia but not limited to families with
schizophrenic offspring. Indeed, this family dynamics is
universal and only when it is extreme does it lead to
schizophrenia.
Some environmental theorists, like Wynne (1970)
and Arieti (1975), have been careful not to exclude any
significant inborn component in the etiology of schizophrenia, and individual variabilities among the potential
schizophrenics are mentioned to account for the differential outcome of individuals exposed to the same
factors.
Another example of a predominantly environmental
and continuum model is that of Manfred Bleuler. Derived from that author's experience with schizophrenics
and their families over several decades and described in
his latest book, M. Bleuler (1972) posits a phenomenological, an outcome, and an etiological continuum. With
regard to etiology, he takes a middle-of-the-road position
between heredity and environment. He rejects any specific schizophrenogenic gene and considers the inheritance to consist of normal genes (found in the rest of
the population) whose combination is "disharmonious"
and is reflected in "disharmony of the tendencies of the
personality." The environmental contribution is also
nonspecific, as none of the experiences to which the
schizophrenic-to-be is exposed are absent from the rest
of the general population.
M. Bleuler goes on to explain why, in his opinion, research on the etiology of schizophrenia has ended in a
blind alley. "Schizophrenia... [is] . . . due to a multiplicity of factors similar to those that play a role in
everyman's development." Most researchers implicitly
assume schizophrenia to be a disease process grafted to
the individual's personality, and this nonheuristic hypothesis, Bleuler maintains, is responsible for the paucity
of data regarding the etiology of schizophrenia.
Any discussion of theories of schizophrenia that
omits Eugen Bleuler leaves itself open to criticism. The
continuum/dichotomy perspective in this paper focuses
on etiological models. E. Bleuler (1950) emphasized the
phenomenology of schizophrenia and the need "to
explain" its symptoms rather than what caused schizophrenia. Nevertheless, E. Bleuler is noncommittal when
he speaks of etiology, as he favors a morbid process involving the brain but does not rule out that "the entire
symptomatology may be psychically determined...
and [may] develop . . . [from] . : . slight quantitative
deviations from the normal" (p. 461).
267
VOL. 3, NO. 2,1977
Comment
Despite their differences, both genetic and environmental etiological models of schizophrenia make common assumptions about the specificity, or lack of specificity, of putative etiological factors. The monogenic
theories (Book 1953, Heston 1970, Kallmann 1946, and
Slater and Cowie 1971) and the environmental theories
of Lidz (1973) and Alanen (1966) assume that a qualitative difference exists between schizophrenics and nonschizophrenics when etiological factors are considered.
The polygenic model (Gottesman and Shields 1973),
the double-bind theory of disease transmission (Bateson
et al. 1956), and M. Bleuler's (1972) model, assumecontrariwise—that a quantitative difference exists between schizophrenics and nonschizophrenics when
etiological factors are considered.
References
Alanen, Y. The family in the pathogenesis of schizophrenic and neurotic disorders. Ada Psychiatrica Scandinavica, 42: Supplement 189, 1966.
Arieti, S. The Interpretation of Schizophrenia. New
York: Basic Books, Inc., Publishers, 1975.
Bateson, G.; Jackson, D.D.; Haley, J.; and Weakland,
J. Toward a theory of schizophrenia. Behavioral Science,
1:251-264,1956.
Bleuler, E. Dementia Praecox or the Group of Schizophrenias. (1911) Translated by J. Zinkin. New York: International Universities Press, Inc., 1950.
Bleuler, M. Conception of schizophrenia within the
last fifty years. International Journal of Psychiatry,
1:501-513,1965.
Bleuler, M. Die schizophrenen Geistesstorungen: Im
Lichte langjahriger Krahken- und Familiengeschichten.
[Schizophrenia Disorders in the Light of Long-term Case
and Family Histories.] Stuttgart: Georg Thieme Verlag,
1972.
Book, J.A. Schizophrenia as a gene mutation. Ada
Geneticae, 4:133-139, 1953.
Falconer, D.S. The inheritance of liability to certain
diseases. Annals of Human Genetics, 29:51-76, 1965.
Freud, S. Neurosis and psychosis. In: Strachey, J.,
ed. The Standard Edition of the Complete Psychological
Works of Sigmund Freud. Vol. 19. London: The Hogarth Press, 1953, p. 152.
Gottesman, 1.1., and Shields, J. Genetic theorizing and
schizophrenia. British Journal of Psychiatry, 122:15-30,
1973.
Heston, L. The genetics of schizophrenic and schizoid
disease. Science, 167:249-256, 1970.
Kallmann, F.J. The genetic theory of schizophrenia.
American Journal of Psychiatry, 103:309-322, 1946.
Kraepelin, E. Dementia Praecox. Huntington, N.Y.:
Robert E. Kreiger Publishing Co:, 1971. p. 256.
Lidz, T. The Origin and Treatment of Schizophrenic
Disorders. New York: Basic Books, Inc., Publishers,
1973.
Meyer, A. The Commonsense Psychiatry of Adolf
Meyer. (Lief, H., ed.) New York: McGraw-Hill, Inc.,
1948. p. 239.
Reich, T.; Cloninger, C.R.; and Guze, S.B. The multifactorial model of disease transmission: I. Description
of the model and its use in psychiatry. British Journal
of Psychiatry, 127:1-10,1975.
Reich, T.; James, J.W.; and Morris, C.A. The use of
multiple thresholds in determining the mode of transmission of semi-continuous traits. Annals of Human
Genetics, 36:163-184, 1972.
Schneider, K. Clinical Psychopathology. New York:
Grune & Stratton, Inc., 1959.
Slater, E., and Cowie, V. The Genetics of Mental
Disorders. London: Oxford University Press, Inc.,
1971. p. 57.
Strauss, J.S., and Carpenter, W.T. Characteristic
symptoms and outcome in schizophrenia. Archives of
General Psychiatry, 30:429-434, 1974.
Sullivan, H.S. Schizophrenia as a Human Process.
New York: W. W. Norton & Co., Inc., 1974. p. 159.
Whitehead, A.N., and Russell, B. Principea Mathematica. Cambridge: Cambridge University Press, 1910.
Wynne, L.C. Communication disorders and the
quest for relatedness in families of schizophrenics.
American Journal of Psychoanalysis, 30:100-114,
1970.
Acknowledgment
Special thanks are due Dr. Ronald O. Rieder for his
helpful comments in the revision of this paper.
The Author
Philippe Khouri, M.D., is a Visiting Research Associate, Laboratory of Psychology and Psychopathology, National Institute of Mental Health,
Bethesda, Md.